Research Article iMedPub Journals Journal of Environmental Research 2019 www.imedpub.com Vol.3 No.1:1 The Chronic Influence of Carbon Monoxide Intoxication on Lipid Peroxidation Agoro ES1*, Ombor JA2, Alabrah PW3 and Tommy EO4 1Enis Biomedical and Forensic Research Institute, Igbogene Epie, Yenagoa, Bayelsa State 2Department of Chemical Pathology, Federal Medical Centre, Yenagoa, Bayelsa State, Nigeria 3Department of Obstetrics and Gynaecology, Federal Medical Centre, Yenagoa, Bayelsa State, Nigeria 4Department of Haematology and Blood Transfusion, Federal Medical Centre, Yenagoa, Bayelsa State, Nigeria *Corresponding author: Agoro ES, Enis Biomedical and Forensic Research Institute, Igbogene Epie, Yenagoa, Bayelsa State, Tel: 08037434995; E- mail: [email protected] Rec date: February 25, 2019; Acc date: March 14, 2019; Pub date: March 23, 2019 Citation: Agoro ES, Ombor JA, Alabrah PW, Tommy EO (2019) The Chronic Influence of Carbon Monoxide Intoxication on Lipid Peroxidation. J Environ Res Vol.3: No.1:1. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free Abstract radicals that damage all components of the cell, including proteins, lipids, and DNA [2]. More severe oxidative stress can Carbon monoxide is a known notorious gas with a high cause cell death and even moderate oxidation can trigger preponderance of causing either morbidity or mortality apoptosis, while more intense stresses may cause necrosis depending on the concentration inhaled or administered. [3,4]. The study was aimed to determine whether chronic CO intoxication could stimulate lipid peroxidation. A total of Carbon monoxide (CO) is a poisonous, colourless, tasteless, twenty albino rabbits of same sex, age and weight odourless and non-irritant gas produced by incomplete constituted the sample size as validated by the Mead’s combustion of organic material due to insufficient oxygen formula. The study was divided into four groups of five supply to enable complete oxidation to carbon dioxide (CO2) rabbits each; the control, 10 days, 20 days and 30 days [5]. It utilizes hypoxia in exerting its nefarious effect on the respectively. Except the control group, others were entire body system by making oxygen inaccessible. exposed daily to thirty minutes of 200 ppm CO intoxication. The statistical analysis was done with the aid Carbon monoxide poisoning is the inhalation of large of SPPS 20 version, using One-way Anova (Post Hoc-LSD). quantity of CO that is deleterious to the body. It could be acute Biochemical parameters indicative of lipid peroxidation or chronic depending on the concentration inhaled. Chronic were analysed using blood and vitreous humor samples. CO poisoning involves the inhalation of abnormal The serum and vitreous chemistry revealed a significant concentration of CO that cannot lead to immediate death over decreased (p<0.05) in the concentrations of total a period of time exceeding one month. cholesterol, high density lipoprotein, low density Lipid peroxidation is studied with the aid of biochemical lipoprotein, very low density lipoprotein, uric acid, parameters that are affected or that cushion the effects of free Glutathione Reductase and Superoxide Dismutase. On the contrary, the concentration of serum and vitreous MDA radicals. Such parameters include malonaldehyde, glutathione increased significantly (p<0.05). The findings revealed that reductase, superoxide dismutase, catalase, uric acid, and lipid chronic CO intoxication could provoke lipid peroxidation. profiles. These biochemical parameters to a large extend could be altered as a result of lipid peroxidation. Keywords: Free radicals; Malondialdehyde; Superoxide The effect of lipid peroxidation is not new in biomedical dismutase; Catalase; Uric acid science. The alterations arising from the above stated biochemical parameters by acute CO intoxication is very revealing as posited by Agoro et al. [6]. In carbon monoxide Introduction poisoned patients, an altered balance between reactive oxygen species and antioxidant concentrations has been Lipid peroxidation is the oxidative degradation of lipids. It is reported [7]. Also it has been observed that free radicals and the process in which free radicals "steal" electrons from the oxidative stress are among factors involved in pathogenesis of lipids in cell membranes, resulting in cell damage. This process acute carbon monoxide poisoning [8]. Another author held a usually proceeds by a free radical chain reaction mechanism. strong relationship between acute carbon monoxide poisoning The reaction consists of three major steps: initiation, and free radical and [9]. Egwurugwu et al. did a work on gas propagation, and termination. The chemical products of this flaring in the Niger Delta of Nigeria using human subjects and oxidation are known as lipid peroxides or lipid oxidation revealed that serum concentrations of triglycerides, low products (LOPs) [1]. density lipoprotein (LDL) and very low density lipoprotein © Copyright iMedPub | This article is available from: http://www.imedpub.com/journal-environmental-research/inpress.php 1 Journal of Environmental Research 2019 Vol.3 No.1:1 (VLDL) were elevated as compared to the control, whereas Collection of vitreous humor high density lipoprotein (HDL) decreased [10]. Vitreous humor samples were collected by the method of Nigerians are exposed to varying degrees of CO due to the Coe [13]. In brief, within 30 min of euthanization, samples high demand of CO-producing machines and equipment. A were collected by insertion of a 27-G needle into the cantus of deliberate study of the effect of chronic exposure to CO on the eye and ≈ 1 ml was then retrieved into a plane tube. Only lipid peroxidation parameters will in no measure shaping the clear liquid free of any tissue contaminants/fragments was perspective to several diseases linked to lipid alterations. The acceptable for analyses. Each isolated vitreous samples was products of this study could be useful in policy enactment in centrifuged at 2050 rpm (10 min, 25°C) and resultant combating chronic diseases, preventing avoidable epidemics supernatants were collected for the analyses. and enhancing medical well-being. Collection of cardiac blood Materials and Methods At necropsy, blood samples were collected from the heart using the method of Ness [14]. In brief, within 30 min of Study area euthanization, samples were collected by insertion of a 27-G The animal intoxication was carried out in the animal into the left side of the chest, through the diaphragm, from the science laboratory of the Niger Delta University. Similarly, the top of the sternum. Blood was then slowly withdrawn into a biochemical analysis took place at the Chemical Pathology plane tube. The samples were allowed to clot at room Laboratory of the Niger Delta University Teaching Hospital, temperature and then serum was collected by centrifugation Okolobiri, Bayelsa State. at 2000 rpm for ten minutes at 25°C for use in biochemical analyses. Animals Bio-analyses New Zealand white albino rabbits (male, 6-8-mo-of-age, 1.5-2.0 kg) were obtained from Imo State in Nigeria. Rabbits The vitreous or serum CAT activity was assayed according to used were apparently healthy and active as confirmed and the method of Aebi [15]. The activity of serum superoxide approved by a university veterinarian. Each was housed in an dismutase (SOD) was assayed by the method of Xin et al. as individual cage in a specific pathogen-free facility maintained contained in Randox commercial kit leaflet [16]. Lipid peroxid at 25°C with a 60% relative humidity and a 12 hrs light/dark analyses was carried out by determining the concentration of cycle. All rabbits had ad libitum access to standard rabbit chow MDA formed using the method of Varshney and Kale [17]. bought in Yenagoa, Bayelsa State and filtered water. Any rabbit The concentration of glutathione was determined according showing signs or symptoms of illness prior to exposures were to the method of Habig et al. [18]. Vitreous or serum uric acid excluded from the research. Ultimately, a total of 20 rabbits concentration was estimated quantitatively by Uricase Method were used for the exposures/analyses. using Agappe kit as specified by Agappe Diagnostics After two weeks of acclimatization, the rabbits were (Switzerland) (Agappe Kit Leaflet). Vitreous or plasma total randomly allocated into four groups. The first group was cholesterol, triglyceride, HDL concentrations were estimated designated controls that were exposed to air only (n=5). The quantitatively using Agappe kit as specified by Agappe remaining three groups of rabbits were exposed daily whole- Diagnostics (Switzerland) (Agappe Kit Leaflet). Vitreous or body to CO for 30 min for 10, 20, or 30 days (n=5/group). All plasma LDL and VLDL concentration was derived animals were exposed in a CO chamber. The source of the CO mathematically by the formular as stated by Carl and Edward, was a portal Sumac generating set. All CO levels were and Friedewald et al. [19,20] respectively. constantly monitored using a Carbon Monoxide Meter Gasman-CO (PCE Instrument, UK). Exposure levels were never Statistical analysis greater than 200 ppm in the chamber. This level was selected All data were reported as means ± Standard Deviation. A based on earlier studies of Goldstein and Struttmann et al. one-way analysis of variance [ANOVA) followed by a Fisher's wherein 200 ppm was found to reflect CO concentration that Least Significant Difference (LSD) post-hoc